Published online Feb 15, 2019. doi: 10.4251/wjgo.v11.i2.91
Peer-review started: November 14, 2018
First decision: December 7, 2018
Revised: December 22, 2018
Accepted: January 8, 2019
Article in press: January 8, 2019
Published online: February 15, 2019
Long non-coding RNAs (lncRNAs) are a class of non-coding and single-stranded RNAs, with the length of more than 200 nucleotides. Although lncRNAs have no protein-coding capacity, they take part in the regulation of gene expression at the post-transcriptional level. Recent studies have found that lncRNAs are involved in the initiation and development of cancers, including gastric cancer (GC). To identify and explore the potential role of lncRNAs in GC could contribute to finding a promising biomarker in the diagnosis, therapy, and prognosis management of GC.
GC is a malignant digestive system tumor with high incidence and mortality in the world. Considering the actual mechanisms of lncRNAs in GC remain unclear, it is urgent to identify and explore the potential role of lncRNAs. The finding of novel lncRNA could contribute to studying the initiation and development mechanisms of GC.
In the study, we aimed to identify a novel lncRNA and explore its biological effect in GC. Once its actual role is confirmed, it could be a promising molecule in studying the diagnosis, therapy, and prognosis management of GC. The potential microRNAs (miRNAs) that LINC02532 may sponged were also predicted by bioinformatics. The results are useful for further exploring the mechanisms of competing endogenous RNAs (ceRNA).
We first identified differentially expressed genes by processing the RNA-Seq or mature miRNAs sequencing data of GC downloaded from The Cancer Genome Atlas or Firebrowse website. The RNA-Seq data supported that LINC02532 was upregulated and its expression level in GC cells and tissues was confirmed by qRT-PCR assay. The functional assays indicated that LINC02532 promoted GC cells proliferation, migration, and invasion in vitro. RNA22 tool was selected for predicting target miRNAs, which may be sponged by LINC02532. The miRNA target genes were obtained by the TargetScan, miRDB, and DIANA software. The gene functional enrichment analysis of the common target genes was performed by the Database for Annotation, Visualization, and Integrated Discovery tool.
We identified that LINC02532 was upregulated in GC and promoted GC cell proliferation, migration, and invasion in vitro. The results of statistical analysis showed that a high expression of LINC02532 was associated with high TNM stage and poor differentiation. Besides, Kaplan-Meier survival analysis based on The Cancer Genome Atlas data indicated that patients with higher LINC02532 expression had poorer prognosis than those with lower LINC02532 expression. Furthermore, we found that LINC02532 may act as a ceRNA by sponging miR-129-5p and miR-490-5p. The target genes of the two miRNAs were selected for gene functional enrichment analysis and the results supported the potential oncogene role of LINC02532 in GC.
We found that novel LINC02532 was significantly upregulated in GC, and it may act as an oncogene to promote the tumorigenesis of GC. The present study revealed that LINC02532 could be a promising target in the diagnosis, therapy, and prognosis management of GC.
The present study was well designed by combining bioinformatics prediction with experimental evidence. Furthermore, we will further focus on the mechanisms of LINC02532, such as the ceRNA hypothesis.